Abstract
While over the past decades T cells have been considered key players in the pathogenesis of multiple sclerosis (MS), it has only recently become evident that B cells have a major contributing role. Our understanding of the role of B cells has evolved substantially following the clinical success of B cell-targeting therapies and increasing experimental evidence for significant B cell involvement. Rather than mere antibody-producing cells, it is becoming clear that they are team players with the capacity to prime and regulate T cells, and function both as pro- and anti-inflammatory mediators. However, despite tremendous efforts, the target antigen(s) of B cells in MS have yet to be identified. The first part of this review summarizes the clinical evidence and results from animal studies pointing to the relevance of B cells in the pathogenesis of MS. The second part gives an overview of the currently known potential autoantigen targets. The third part recapitulates and critically appraises the currently available B cell-directed therapies.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS)
This review summarizes the clinical evidence and results from animal studies pointing to the relevance of B cells in the pathogenesis of MS
While the experimental model for MS, i.e., the adoptive transfer of activated encephalitogenic T cells leading to demyelination, promoted the notion that MS is a T cell-mediated disease for a long time, it was recently elegantly shown that the B cell antigen-presenting (APC) function is crucial for the induction of myelin oligodendrocyte glycoprotein (MOG)-induced EAE
Summary
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Both experimental and clinical evidence suggest that it is initiated by autoreactive immune cells directed. This review summarizes the clinical evidence and results from animal studies pointing to the relevance of B cells in the pathogenesis of MS. It gives a detailed overview of the currently known potential autoantigen targets. This knowledge provides the basis to understand the rationale behind B cell-directed therapies that are discussed in the third part
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